Thursday, September 1, 2016

A 60-something woman had syncope and was unconscious for a few minutes. It was not a seizure. EMS found her lethargic and short of breath but without chest pain. Pulse was 103, BP 100/60, and O2 saturation on room air 98%.

She was brought to the ED, where her SpO2 was 93%, BP 88/48, pulse 100.

On arrival in the ED, she underwent an immediate bedside cardiac ultrasound:

What do you see?

There is a very large RV and very poor LV filling; the LV ejection fraction is nearly 100%. It is easy to jump to the conclusion that this patient has a pulmonary embolism (hypotension, tachycardia, low O2 saturations, syncope, large RV).

An ECG was recorded:

What do you see?

At first glance, this ECG also suggests pulmonary embolism. It shows an S1Q3T3. One might think this is then highly specific for pulmonary embolism. However, S1Q3T3 has a very limited (+) and (-) likelihood ratio for PE; it is seen in only 8.5% of patients with PE and 3.3% of patients who are evaluated for PE but do not have it. See this post for detailed information.

This ECG has quite a bit more information: it shows sinus tachycardia with right axis deviation, a large wide R-wave in V1 (but without complete RBBB), and ST depression with T-wave inversion in V2-V6. This is a typical ECG of right ventricular hypertrophy.

Further history

Further history revealed that the patient had poor po intake and vomiting. Review of records revealed "chronic cor pulmonale" and a review of a previous formal echo showed:

--Pulmonary hypertension .

--Cor pulmonale, severe.

--Normal estimated left ventricular ejection fraction.

--Right ventricular enlargement Marked.

--Decreased right ventricular systolic performance severe

--pulmonary artery pressure: 75 mmHg (normal 15-25)

People with right ventricular hypertrophy due to pulmonary hypertension may have severely decreased RV function and are very susceptible to low preload. Any condition which lowers intravascular volume (such as vomiting and poor po intake) may lead to hypotension and syncope.

In these patients, can volume be assessed with ultrasound imaging of the inferior vena cava (IVC), as is often done in the ED?

No! The pulmonary hypertension will result in a "plump" IVC even with severe volume depletion. The pulmonary hypertension requires high filling pressures (plump IVC) for adequate RV filling.

Physical exam tip: In patients who can stand up, a better measure of volume than IVC is to check orthostatic vital signs and symptoms. In patients who are young and not on beta blockers or calcium channel blockers, the change to an upright position will result in a rise in heart rate to more tachycardic. Older patients or those on such medications will have a drop in BP. If symptomatic, it is pretty specific for volume depletion. The exact numbers are more difficult to specify and beyond the scope of this post, but correction with volume repletion is very good evidence of relative volume depletion.

Case continued

The first troponin returned at 0.090 ng/mL (normal, up to 0.030).

I had just seen this ECG in a stack and knew it was RVH. I had not seen the history yet when the treating physicians sought me out to show me the ECG. Due to the ST depression, echo, and troponin, they were worried about posterior MI or pulmonary embolism. I pointed out that it represents typical findings of chronic RVH due to chronic pulmonary hypertension, not of pulmonary embolism or acute MI. I suggested that this would be typical for an acute exacerbation of severe pulmonary hypertension due to dehydration.

The patient did get a CT pulmonary angiogram for other reasons (suspicion of AV malformation), and it was negative for pulmonary embolism.

Troponin peaked at 0.289 ng/mL. The patient was rehydrated and discharged after a short stay in the hospital.

Although acute coronary syndrome (type 1 Non-STEMI) was not absolutely ruled out, the clinical presentation is typical for dehydration in the setting of pulmonary hypertension and I agree that an angiogram is not necessary.

Comment:

So this episode of volume depletion in the setting of RVH resulted in a type II MI.

You still need to consider PE, but with skepticism. Use d dimer. Do careful history. In this case, the history brought up the likelihood of dehydration. Orthostatics could have confirmed it. Fluid replacement would have resolved the issue. If you're still worried, you may still need CTPA, but your index of suspicion should be much much lower

Excellent case! — albeit one that my opinion about this ECG differs slightly. KEY points brought out by this case (and its accompanying ECG) are the following: i) The HPI ( = History of Present Illness) is an indispensable part of clinical management. This older adult with syncope and initial unresponsiveness had recent poor oral intake and vomiting (ie, a set-up for volume depletion); ii) The PMH ( = Past Medical History) is equally essential to assessment — this patient was found to have chronic cor pulmonale and prior Echo showing marked RVH, pulmonary hypertension but a normal LV; and iii) Use of stat Echo may prove invaluable — great picture here of a markedly dilated hypocontractile RV with associated good LV contractility.

I interpreted this tracing as showing RBBB (or at the least, incomplete RBBB). I measure the QRS as between 0.11-0.12 second (in V1,V2) — with wide terminal S waves in leads I and aVL. Clearly, there are some atypical features here for RBBB — namely lack of an initial upright deflection (r wave) in lead V1, and lack of a wide terminal S wave in lead V6 — but not all RBBBs fit textbook description. Right-terminal delay is suggested by the wide terminal S in limb leads and the tall R in V1. That said, diagnosis of combined RVH and RBBB is challenging under the best of circumstances. Some electrocardiographers suggests excessive height of the R’ deflection in lead V1 (beyond 8, 10 or 15mm) makes that diagnosis — but my reservation has always been that with pure RBBB, the RV depolarizes unopposed, rendering numerical criteria far less objective for detecting true RV chamber enlargement from ECG. Presence of clear RAA in association with a tall R in V1 correlates well with anatomic RVH (since only one condition, which is rare [ = tricuspid stenosis] produces RAE but not RVH) — but the P wave in this tracing lacks the height and pointedness that typically characterizes RAE.

Of note, the QTc in this tracing is LONG — and in my opinion, far longer than should be expected simply from RVH and/or RBBB. In addition, there is ST depression in V2-thru-V5, with what is probably a large U wave in leads V2-thru-V5. This correlates clinically with hypokalemia and the marked hypomagnesemia that this volume-depleted patient had — and further complicates assessment of this ECG.

BOTTOM LINE: Putting all ‘pieces” of the clinical presentation here together — Dr. Smith makes a strong case for primary volume depletion as the precipitating event — which was supported by dramatic clinical improvement with volume repletion. I think it would be hard to be certain as to whether the tracing shown here represents pure RVH (from chronic cor pulmonale with pulmonary hypertension) vs combined conduction defect + RVH — unless one was able to do sequential review of this patients series of prior ECGs over the years to see which ECG features developed when … So while I’ll suggest that we do have evidence of an RV conduction defect here (at the least, incomplete rbbb) — that point is academic, and pales in importance to recognition of how PMH, HPI, Echo in the ED + ECG interpreted in context to the complete clinical situation are the essentials for optimal clinical management. THANKS to Dr. Smith for presenting this excellent case!

Great comments, Ken. thanks. The computer measurement of the QRS was 110 ms (this is one thing computers are accurate at), so incomplete RBBB at best. The QT and QU are indeed long, and much longer than the previous ECG (not shown), and these certainly can be due to low Mg, but K of 3.4 is not very low. RVH is definitely hard to diagnose on ECG in the presence of incomplete RBBB.Steve

Not totally certain, but I suspect there was a period of hypotension from temporary RV failure. This leads to extremely poor RV perfusion (RV is perfused during systole; if there is hypotension at the same time it is pumping against 70 mmHg, there is no perfusion of RV myocardium). Low RV perfusion at the same time that the RV has to pump against very high pulmonary artery pressure leads to some RV myocardial cell loss.

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